The parturition defect in steroid 5alpha-reductase type 1 knockout mice is due to impaired cervical ripening.
The parturition defect in steroid 5alpha-reductase type 1 knockout mice is due to impaired cervical ripening.
复制标题
DOI：
10.1210/mend.13.6.0307
复制
发表时间：
1999-06
影响因子：
--
通讯作者：
M. Mahendroo;Amina Porter;D. Russell;R. Word
中科院分区：
文献类型：
--
作者：
M. Mahendroo;Amina Porter;D. Russell;R. Word
胎儿的成功分娩（分娩）取决于子宫和子宫颈之间的协调相互作用。大多数（70%）缺乏类固醇 5α-还原酶 1 型同工酶的小鼠无法足月分娩，从而表现出分娩缺陷。通过体外和体内测量，我们发现这些突变小鼠在妊娠末期子宫的节律性收缩正常发生。相反，根据生物力学、组织学和内分泌学分析判断，突变动物的子宫颈在足月时未能成熟。妊娠晚期突变小鼠子宫颈中黄体酮代谢受损，导致这种类固醇在组织中积聚。我们得出结论，宫颈成熟失败是缺乏 1 型类固醇 5α 还原酶的小鼠分娩缺陷的基础，并且这种酶通常在妊娠末期宫颈黄体酮分解代谢中发挥重要作用。
Successful delivery of the fetus (parturition) depends on coordinate interactions between the uterus and cervix. A majority (70%) of mice deficient in the type 1 isozyme of steroid 5alpha-reductase fail to deliver their young at term and thus manifest a parturition defect. Using in vitro and in vivo measurements we show here that rhythmic contractions of the uterus occur normally in these mutant mice at the end of gestation. In contrast, the cervix of the mutant animal fails to ripen at term as judged by biomechanical, histological, and endocrinological assays. Impaired metabolism of progesterone in the cervix of the mutant mice in late gestation leads to an accumulation of this steroid in the tissue. We conclude that a failure of cervical ripening underlies the parturition defect in mice lacking steroid 5alpha-reductase type 1 and that this enzyme normally plays an essential role in cervical progesterone catabolism at the end of pregnancy.